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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
15
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pubmed:dateCreated |
2001-8-3
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pubmed:abstractText |
Peripheral insulin resistance and impaired insulin action are the primary characteristics of type 2 diabetes. The first observable defect in this major disorder occurs in muscle, where glucose disposal in response to insulin is impaired. We have developed a transgenic mouse with a dominant-negative insulin-like growth factor-I receptor (KR-IGF-IR) specifically targeted to the skeletal muscle. Expression of KR-IGF-IR resulted in the formation of hybrid receptors between the mutant and the endogenous IGF-I and insulin receptors, thereby abrogating the normal function of these receptors and leading to insulin resistance. Pancreatic beta-cell dysfunction developed at a relative early age, resulting in diabetes. These mice provide an excellent model to study the molecular mechanisms underlying the development of human type 2 diabetes.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-10025399,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-10377413,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-10409618,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-10545524,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-10651265,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-10751208,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-10862794,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-10932232,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-10949030,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-1316361,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-1320041,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-2038318,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-2403659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-2770453,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-7540132,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-7675081,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-7679099,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-8206901,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-8247074,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-8250456,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-8528241,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-8612577,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-8666135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-8712800,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-8981937,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-9389757,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-9421379,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-9486163,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-9806552,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11485987-9844629
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0890-9369
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1926-34
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11485987-Aging,
pubmed-meshheading:11485987-Animals,
pubmed-meshheading:11485987-Blood Glucose,
pubmed-meshheading:11485987-Diabetes Mellitus, Type 2,
pubmed-meshheading:11485987-Fatty Acids, Nonesterified,
pubmed-meshheading:11485987-Glucose,
pubmed-meshheading:11485987-Glucose Clamp Technique,
pubmed-meshheading:11485987-Humans,
pubmed-meshheading:11485987-Hyperinsulinism,
pubmed-meshheading:11485987-Insulin,
pubmed-meshheading:11485987-Insulin Resistance,
pubmed-meshheading:11485987-Islets of Langerhans,
pubmed-meshheading:11485987-Liver,
pubmed-meshheading:11485987-Mice,
pubmed-meshheading:11485987-Mice, Transgenic,
pubmed-meshheading:11485987-Muscle, Skeletal,
pubmed-meshheading:11485987-Mutagenesis, Site-Directed,
pubmed-meshheading:11485987-Prediabetic State,
pubmed-meshheading:11485987-Receptor, IGF Type 1,
pubmed-meshheading:11485987-Receptor, Insulin,
pubmed-meshheading:11485987-Triglycerides
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pubmed:year |
2001
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pubmed:articleTitle |
Functional inactivation of the IGF-I and insulin receptors in skeletal muscle causes type 2 diabetes.
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pubmed:affiliation |
Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health, Bethesda, Maryland 20892, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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